Anti-tumor therapy

Wang CY, Cusack JCJr, Liu R, Baldwin ASJr (1999b) Control of inducible chemore-sistance enhanced anti-tumor therapy through increased apoptosis by inhibition of NF-kappaB. Nat Med 5 412-417... 

Friedrich J, Ebner R, Kunz-Schughart LA (2007) Experimental anti-tumor therapy in 3-D spheroids—old hat or new challenge Int JRadiatBiol 83 849-871... 

Schlaeppi JM, Wood JM. Targeting vascular endothelial growth factor (VEGF) for anti-tumor therapy, by anti-VEGF neutralizing monoclonal antibodies or by VEGF receptor tyrosine kinase inhibitors. Cancer Metastasis Rev 1999 18 4734-81. 

It follows that for realization of effective anti-tumoral therapy one should select such chemical agent x which action on atypical cells in many times exceeds its influence on normal ones, i.e. 3, 64 81, 82. by such effect one may significantly reduce stationary value... 

Recent studies have revealed that the human tumor viruses EBV, HHV-8, human papillomavirus, HBV, HCV, and HTLV-1 express proteins that are targeted to the mitochondria (8). Because the mitochondria play a critical role in energy production, cell death, calcium homeostasis, and redox balance, these proteins have profound effects on host cell physiology. Further study of these proteins and their interactions with mitochondria will aid in the understanding the mechanisms of viral replication and tumorigenesis and could reveal important new targets for anti-tumor therapy. 

Since antibodies, by their nature, bind to antigens, their function is often to augment intrinsic clearance mechanisms, as well as potentially exerting definitive therapeutic effects themselves. It is not surprising, therefore, that the therapeutic targets for antibody therapy are extremely broad, ranging from anti-tumor therapy to specific immunological... 

Marker JM. Biologic warfare for a good cause HSV-1 anti-tumor therapy. Clin Neurosurg 2004 51 73-80. 

Li[BH4] reacts with a tenfold excess of B4CI4 to B5H9 and BgHio in 63 and 19% yield, respectively, in addition to H2 [1]. Na[BH4] may be conveniently converted to [HN(C2Hs)3]2-[B12H12] by treatment with five equivalents of BH3-N(C2H5)3 at 1 atm pressure in a method developed for the isolation of boranes for neutron-capture anti-tumor therapy [2]. 

The high concentration of NO which is induced by activated macrophages may be cytostatic or cytotoxic for tumor cells. Lipopolysaccharide (LPS) or some cytokines such as TNF-a and IFN-y can efficiently regulate iNOS transcription by activation of nuclear factors such as NF-kB and AP-1. Thus, macrophage activation to induce high concentration of NO by LPS or some cyotokines is a candidate for anti-tumor therapy. 

It is currently difficult to regulate localization of NO production by the systemic administration of NO donors. The manipulation of NO donors in tumor tissues also requires research. There is a large variety of potential NO donors that may allow for localization in tumor tissues. It can be anticipated that there will be a new era for anti-tumor therapy that employs NO in combination therapies with radiation, chemotherapeutic agents, and cytokines for conventional therapy-resistant tumors. 

Rapamycin and its close chemical relatives can almost be called a molecule for most diseases since the rapamycins now cover molecules that have biological properties ranging from initial anti fungal activities through immunomodulation to anti-tumor therapies, and even as a molecule to use in stents to avoid plaque formation in blood circulation. 

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